In the years immediately following, preclinical inquiries commenced to suggest that all treatments effective against depression, namely ADs, sleep deprivation and electroconvulsive therapy, could increase the expression of a neurotrophin, the so-called brain-derived neurotrophic factor (BDNF) and its receptor (tropomyosin receptor kinase B, TrkB) in the rat hippocampus [5,6]. This evidence concerns the gene BDNF and depressive symptom measurement.